Abstract
Although Niemann-Pick C1 disease has frequently been called "juvenile Alzheimer's", the effects of introducing Npc1 mutations into a mouse model of Alzheimer's have not previously been performed. We have crossed Npc1 (+/-) mice with APP/PS1 "Alzheimer's" mice and studied Aβ42 accumulation and amyloid plaque formation. Mice heterozygous for Npc1 and positive for the APP and PS1 transgenes accumulated Aβ42 more rapidly than the APP/PS1 controls and this correlated, as expected, with the area of amyloid plaques. We conclude that the alterations of intracellular cholesterol present in Npc1 (+/-) mice can influence the progress of Alzheimer's disease in the APP/PS1 mouse model.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Age Factors
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Alzheimer Disease / genetics*
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Alzheimer Disease / pathology
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Amyloid beta-Peptides / metabolism
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Animals
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Benzothiazoles
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Brain / metabolism
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Brain / pathology
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Disease Models, Animal
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Humans
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Intracellular Signaling Peptides and Proteins
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Mice
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Mice, Transgenic
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Niemann-Pick C1 Protein
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Niemann-Pick Diseases / genetics
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Niemann-Pick Diseases / pathology
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Peptide Fragments / metabolism
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Plaque, Amyloid*
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Proteins / genetics*
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Regression Analysis
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Thiazoles / metabolism
Substances
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Amyloid beta-Peptides
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Benzothiazoles
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Intracellular Signaling Peptides and Proteins
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Niemann-Pick C1 Protein
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Npc1 protein, mouse
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Peptide Fragments
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Proteins
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Thiazoles
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amyloid beta-protein (1-42)
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thioflavin T